fatty acid synthesis Flashcards

exam 3

1
Q

FAS occurs in the

A

liver and adipose

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2
Q

FAS occurs also in the mammary glands but during

A

lactation

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3
Q

FAS subcellular location is in the

A

cytoplasm

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4
Q

Citrate in the cytoplasm will favor

A

FAS

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5
Q

FAS uses Acetyl-CoA, but Acetyl-CoA is made in the

A

mitochondria

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6
Q

_________ combines Acetyl-CoA and OAA to form _____

A

Citrate synthase combines Acetyl- CoA and OAA to form Citrate

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7
Q

Once citrate passes to cytoplasm ______ cleaves citrate to OAA and Acetyl CoA

A

citrate lyase

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8
Q

the coenzyme for Acetyl CoA carboxylase

A

Biotin

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9
Q

first reaction of FAS

A

reaction of acetyl-CoA + HCO3- to make malonyl CoA

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10
Q

FAS rate limiting step and why?

A

the conversion between acetyl-CoA to malonyl-CoA is the rate limiting step—> consumes ATP

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11
Q

ACC enzyme is active as a

A

polymer

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12
Q

Citrate does what towards ACC?

A

increases polymerization

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13
Q

insulin does what towards ACC?

A

activates protein phosphatase which also increases polymerization

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14
Q

ACC is inactive as a

A

protomer

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15
Q

palmitoyl CoA does what towards ACC?

A

will depolymerize ACC because it is a product of FAS

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16
Q

Glucagon and Epinephrine does what towards ACC?

A

activates CAMPK to phosphorylate ACC and depolymerize

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17
Q

Fatty acid synthase is regulated both with

A

hormone and substrate

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18
Q

Fatty acid synthase creates fatty acids with __________, _________ and ___ to form FA chains

A

Acetyl-CoA, malonyl- CoA and NADPH

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19
Q

Fatty acid synthase increases with ____ meal

A

carbohydrate rich meal

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20
Q

Fatty acid synthase is regulated by transcription factors _____ and ______

A

ChREBP and SREBP

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21
Q

G6P, F26BP and X5P ________ levels of ChREBP and thus _______ transcription of Fatty acid synthase

A

increases levels of ChREBP and thus increases transcription of Fatty acid synthase

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22
Q

Insulin or IGF will _________ levels of SREBP and will _________ Fatty acid synthase transcription

A

increase levels and activate transcription

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23
Q

the two prosthetic group of Fatty acid synthase

A
  1. sulfhydryl

2. phosphopantetheine

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24
Q

Fatty acid synthase is a dimer of 2 polypeptides, each with ____ enzymatic activities

A

7

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25
Q

in humans, Fatty acid synthase is _____ but in lower organism it has ________

A

human= single organism

lower org. = several individual proteins

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26
Q

Phosphopantetheine is covalently linked to serine of

A

acyl carrier protein of Fatty acid Synthesis

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27
Q

what allows for with the long arm of Phosphopantetheine?

A

thiol to move from one site to another

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28
Q

Fatty acid Synthesis is a ____ metabolic pathway..?

A

spiral because it uses the same set of reactions until product is made

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29
Q

what is NADPH is used for Fatty acid Synthesis?

A

reduction and anabolism

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30
Q

where is NADPH derived? (2)

A

oxidative Phase of PPS and NAPH linked malate DH

31
Q

condesing enzyme in Fatty acid Synthesis releases ____by a _____ rxn

A

CO2 by a decarboxylase reaction

32
Q

B-keto reductases uses _______ for reduction

A

NADPH

33
Q

Dehydratase removes _____ and forms a

A

removes H2O and forms a double bond

34
Q

enoyl-reductase reduces the double bond to an _____ bond using ______

A

double bond to an alkane bond using NADPH

35
Q

growing fatty acid chain is on

A

ACP

36
Q

cleaves off palmitate is until Fatty acid Synthesis is needed for another fatty acid

A

thioesterase

37
Q

Thioesterase II

A

cleaves FA around 8-14 in lactating mammary glands

38
Q

overall requirments for FA synthesis:

_____ Acetyl-CoA
_____ ATP to make Malonyl CoA
_____ NADPH

A

8 Acetyl-CoA
7 ATP to make Malonyl CoA
14 NADPH

39
Q

inhibits Beta oxidation

A

malonyl-CoA

40
Q

Malonyl-CoA inhibits what enzyme in beta oxidation?

A

CAT-1

41
Q

_____ will inhibit FAS by phosphorylating and inhibiting ACC

A

AMPK

42
Q

Adds 2C to carboxyl end, followed by reduction and dehydration

A

elongases

43
Q

eloganses changes w#?

A

NO

44
Q

Add cis double bonds, spaced 3 C away and never closer than w7

A

desaturases

45
Q

oxidize PUFA to create intercellular messengers

A

oxygenases

46
Q

Add-OH to alpha carbon of FAs in nervous tissue

A

Hydroxylases

47
Q

Where does FA elongation occurs?

A

on the smooth ER or Matrix

48
Q

desaturases add cis bonds but never closer than ____ and never past

A

w-7 and never past C9

49
Q

Reduction to B-OH via

A

NADPH

50
Q

reduction to stearoyl-CoA using

A

NADPH

51
Q

W3/w6 serve as precursors for singaling molecules such as

A

prostaglandins and leukotrienes

52
Q

linoleic acid creates

A

PG1 and PG2

53
Q

alpha-linolenic creates

A

PG3

54
Q

Formation of TAG:

loss of Pi forms

A

DAG

55
Q

Formation of TAG:

DGAT adds last

A

acyl-CoA to from TAG

56
Q

Formation of TAG

committed step of TAG synthesis?

A

DGAT step [diglyceride acyltranserase]

57
Q

Formation of TAG:

dietary formation of DAG from acyl-CoA to 2MAG

A

MGAT

58
Q

Formation of TAG:

Glycerol-3-Phosphate acyltransferase adds

A

phosphatidate

59
Q

lypolysis

A

liver

60
Q

glycolysis

A

adipose

61
Q

glycerol kinase is absent in

A

adipose

62
Q

Both Beta- Oxidation and TAG synthesis requires

A

activation of FA with CoA

63
Q

activates FAs

A

acyl-CoA synthetase

64
Q

FAs cannot be used for

A

gluconeogenesis

65
Q

ketones produce __________ from fats for ____ when glucose is not present

A

ketones produce soluble energy from fats for brain when glucose is not present

66
Q

most tissues are getting energy from __________ when glucose levels are low in the blood and glycogen stores are depleted

A

FA oxidation

67
Q

which organ converts FAs to Ketone Bodies which can then move freely through blood and brain

A

liver

68
Q

[2] molecules that act as ketone bodies and are soluble in the blood

A
  1. acetoaetate

2. 3-hydroxybutyrate

69
Q

does the liver use some of the ketone bodies it produces?

A

NOOOOOOOOOOOOOOOO

70
Q

which enzyme breaks down ketone bodies?

A

thiophorase

71
Q

where is thiophorase not found?

A

liver

72
Q

buildup of ketone bodies leads to

A

ketoacidosis

73
Q

trets refractory epilepsy, PHD defects and GLUT1 defects

A

ketogenic diet